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We demonstrate that mutation ofxerC , which reportedly encodes a homologue of anEscherichia coli recombinase, limits biofilm formation in the methicillin-resistantStaphylococcus aureus strain LAC and the methicillin-sensitive strain UAMS-1. This was not due to the decreased production of the polysaccharide intracellular adhesin (PIA) in either strain because the amount of PIA was increased in a UAMS-1xerC mutant and undetectable in both LAC and its isogenicxerC mutant. Mutation ofxerC also resulted in the increased production of extracellular proteases and nucleases in both LAC and UAMS-1, and limiting the production of either class of enzymes increased biofilm formation in the isogenicxerC mutants. More importantly, the limited capacity to form a biofilm was correlated with increased antibiotic susceptibility in both strains in the context of an established biofilmin vivo . Mutation ofxerC also attenuated virulence in a murine bacteremia model, as assessed on the basis of the bacterial loads in internal organs and overall lethality. It also resulted in the decreased accumulation of alpha toxin and the increased accumulation of protein A. These findings suggest thatxerC may impact the functional status ofagr . This was confirmed by demonstrating the reduced accumulation of RNAIII and AgrA in LAC and UAMS-1xerC mutants. However, this cannot account for the biofilm-deficient phenotype ofxerC mutants because mutation ofagr did not limit biofilm formation in either strain. These results demonstrate thatxerC contributes to biofilm-associated infections and acute bacteremia and that this is likely due toagr -independent and -dependent pathways, respectively.

XerC Contributes to Diverse Forms of Staphylococcus aureus Infection via agr -Dependent and agr -Independent Pathways